Despite recent advances in surgical techniques, adhesion formation remains a leading cause of persistent infertility following reconstructive tubal surgery. Recently, we reported that reduction of fibroproliferative inflammation by nonsteroidal anti-inflammatory drugs was an effective method of modifying peritoneal healing. Although the pharmacologic activity of these drugs is mediated through arachidonic acid metabolism, their mechanism of action in altering postoperative peritoneal healing remains unknown. In this grant, we plan to determine the cellular events leading to postoperative adhesion formation and at what point nonsteroidal anti-inflammatory drugs modify this process. In specific, we plan to perform the following studies in a dose-response and time response format: 1) Identification of the changing cellular patterns accompanying the formation of adhesions during re-epithelialization and the results of pharmacologic pertubation of fibroproliferative inflammation on that response. 2) Determine the pattern of arachidonic acid metabolism, collagen and proteoglycan secretion in cellular elements central to peritoneal re-epithelialization with and without inhibitors of arachidonic acid metabolism or corticosteroids. 3) Quantitative assessment of de novo inflammation in vivo (using eye chamber) to explant postoperative peritoneal repair cells and the effects of pharmacologic modifiers of arachidonic acid metabolism on that response. Through elucidation of the biochemical events and cellular elements involved in adhesion formation and their respective responses to pharmacologic manipulations, strategies should be forthcoming allowing the design of clinically effective methods for adhesion-free surgery.